Without sounding stupid, it is difficult to define the term "sympathomimetic" without discussing how these drugs mimic the physiological effects of stimulating the sympathetic nervous system. This is in fact the widely accepted definition, and it includes both drugs which are direct agonists of monoamine receptors (eg. adrenaline), drugs which have indirect action at those synapses (eg. amphetamines), drugs which modulate the sympathetic nervous system indirectly (such as caffeine) and drugs which are sympathetic depressants but for which the withdrawal syndrome is sympathomimetic (such as benzodiazepines and baclofen).
That's a fairly wide net to cast for a quick revision resource. Particularly where the college does not seem particularly interested in three quarters of the toxicology spectum abovementioned. The only sympathomimetic toxicity question has been about methamphetamine (Question 11 from the first paper of 2018), which is surprising because in Australia amphetamine toxicity has the second highest mortality among illicit substances, second only to heroin (Li & Gunja, 2012). Deaths from methamphetamine specifically have doubled in the period between 2009 to 2015. Generally speaking, it seems like something ICU trainees should be familiar with.
In terms of published peer-reviewed resources, there is much to choose from. An excellent review hanging off a case report is offered by Williams et al (2018), and probably contains enough to score a passing mark. For a more extensive and academic treatment, one can be directed to the systematic review by Richards et al (2015). Local management recommendations are available (Jenner et al, 2006) but are somewhat dated.
Not only intoxication, but also withdrawal from sympathetic suppressants can give rise to a sympathomimetic toxidrome picture
It is surprising to see caffeine up there, but it can produce this toxidrome in vast doses (Laitselart et al, 2018)
Control of agitation is the main clinical priority. If you control agitation, you will also ameliorate the cardiovascular effects and risk of haemorrhagic stroke.
Respiratory
Circulatory
Neurological
Fluid, electrolyte and endocrine-related
Renal
When ingested orally methamphetamine concentration peaks after 2-4 hours. When injected or smoked, the peak effect is obviously immediate. These drugs arre all highly lipophilic and have large volumes of distribution. Because they differ structurally from catecholamines (i.e. they have no OH groups on their phenyl ring) these substances are not susceptible to metabolism by COMT or MAO.
Amphetamines in general undergo all sorts of complex metabolic modification, and are therefore cleared predominantly by the liver. Methamphetamine specifically has a relatively long half-life (19-34 hours is the figure given by Goldfranks' Manual).
The effects of amphetamines are exerted by a number of mechanisms:
Methamphetamine lack the capacity to activate noradrenaline receptors directly. Most of its effect is exerted indirectly, by displacing noradrenaline (as well as dopamine and serotonin) from presynaptic storage vesicles. It also inactivates the catecholamine reuptake transporters. The consequence of this is increased neurotransmitter presence in the synapse. This relates to the toxicty: the cardiovascular effects are predominantly due to noradrenaline displacement, the behaviour alteration and psychotic symptoms are likely due to the dopamine, and serotonin is held responsible for the mood alteration and bizarrely distorted response to thirst and hunger. The selectivity for reuptake transporters determines much of the pharmacological effects; for instance MDMA is much more selective for the serotonin reuptake transporter and therefore manifests predominantly serotonergic effects.
Decontamination
Control of agitation
Control of hypertension
Seiziure management
Temperature management
Fluid and electrolyte correction
Li, Wenlong, and Naren Gunja. "Illicit drug overdose: Prevalence and acute management." Australian family physician 42.7 (2013): 481.
Vasan, Sarayu, and Garth J. Olango. "Toxicity, Amphetamine." (2017).
Richards, John, and Erik Laurin. "Toxicity, methamphetamine." (2017).
Darke, Shane, Sharlene Kaye, and Johan Duflou. "Rates, characteristics and circumstances of methamphetamine‐related death in Australia: a national 7‐year study." Addiction112.12 (2017): 2191-2201.
Albertson, Timothy E., Robert W. Derlet, and Brent E. Van Hoozen. "Methamphetamine and the expanding complications of amphetamines." Western Journal of Medicine 170.4 (1999): 214.
King, Andrew, Mirjana Dimovska, and Luke Bisoski. "Sympathomimetic Toxidromes and Other Pharmacological Causes of Acute Hypertension." Current hypertension reports20.1 (2018): 8.
Laitselart, Philippe, et al. "Severe Sympathomimetic Toxidrome in a French Soldier: How Caffeine Overdose Can Lead to Severe Consequences." Military Medicine (2017).
Richards, John R., et al. "Treatment of toxicity from amphetamines, related derivatives, and analogues: a systematic clinical review." Drug & Alcohol Dependence 150 (2015): 1-13.
Jenner, L., et al. "Management of patients with psychostimulant toxicity: guidelines for emergency departments." Canberra, Australian Government Department of Health and Ageing (2006).